title: Chronic progressive deficits in neuron size, density and number in the trigeminal ganglia of mice latently infected with herpes simplex virus.
abstract: Numerous epidemiological studies have proposed a link between herpes simplex virus (HSV) infection and several common chronic neuropsychiatric and neurodegenerative diseases. Experimental HSV infection of mice can lead to chronic behavioral and neurological deficits and chronic pain. While neuron injury and loss are well-documented consequences of the acute phase of infection, the pathologic consequences of latent HSV infection are poorly understood. To determine whether latent HSV infection can cause neuronal injury in mice, trigeminal ganglia (TG) derived from adult BALB/c mice 1, 12 and 31 weeks after corneal HSV type 1 (HSV-1) inoculation were analyzed for evidence of productive or latent HSV-1 infection, inflammation and changes in neuron size, density and number. We found that latent HSV-1 infection between 12 and 31 weeks after corneal virus inoculation was associated with inflammation and progressive deficits in mean neuron diameter, neuronal nucleus diameter, neuron density and neuron number in the TG relative to mock-infected controls. The extent of neuronal injury during latent infection correlated with the extent of inflammation. These studies demonstrate that latent HSV infection is associated with progressive neuronal pathology and may lead to a better understanding of the role of HSV infections in chronic neurological diseases.
authors.affiliation: Department of Pathology, University of Illinois at Chicago, College of Medicine, Chicago, IL 60612, USA.
authors.forename: Sandor
authors.initials: S
authors.lastname: Dosa
authors.forename: Karla
authors.initials: K
authors.lastname: Castellanos
authors.forename: Sarolta
authors.initials: S
authors.lastname: Bacsa
authors.forename: Eva
authors.initials: E
authors.lastname: Gagyi
authors.forename: S Krisztian
authors.initials: SK
authors.lastname: Kovacs
authors.forename: Klara
authors.initials: K
authors.lastname: Valyi-Nagy
authors.forename: Deepak
authors.initials: D
authors.lastname: Shukla
authors.forename: Terence S
authors.initials: TS
authors.lastname: Dermody
authors.forename: Tibor
authors.initials: T
authors.lastname: Valyi-Nagy
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D002452:Cell Count / Q000379:methods; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D015967:Gene Expression Regulation, Viral; D015658:HIV Infections / Q000473:pathology*; D018259:Herpesvirus 1, Human / Q000472:pathogenicity*; D007249:Inflammation / Q000209:etiology / Q000821:virology; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000473:pathology* / Q000821:virology; D010750:Phosphoproteins / Q000378:metabolism; D013997:Time Factors; D012668:Trigeminal Ganglion / Q000473:pathology* / Q000821:virology; D014764:Viral Proteins / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C491734:Lat protein, mouse; D008565:Membrane Proteins; D010750:Phosphoproteins; D014764:Viral Proteins